The proposed research is concerned with mechanisms underlying the recovery of motor behavior after damage to spinal cord pathways in the adult cat. Quantitative kinematic analysis will be carried out to determine the rate and extent of recovery of locomotion and postural reflexes after damage to descending pathways or to dorsal root afferents. The first hypothesis is that the extent of recovery of motor behavior will be enhanced by reducing the initial degree of depression (spinal shock) that occurs after spinal transection. One side of the cord will be protected from spinal shock by making a chronic unilateral lesion prior to transection. Greater recovery on the side with prior hemisection than on the "acute" side (intra-animal comparison) would support the hypothesis. Greater recovery in this preparation than after transection alone (inter-animal comparison) would also provide support for the hypothesis. The second hypothesis concerns recovery of motor behavior after deafferentation. Preliminary results indicate that after unilateral hindlimb deafferentation, although overground and quadrupedal locomotion recover, bipedal locomotion does not recover. This failure is hypothesized to be due to descending inhibitory influences. Therefore, enhanced recovery of bipedal locomotion in the deafferented limb after subsequent destruction of descending pathways or pharmacological blockade of inhibitory systems would support the hypothesis. The third hypothesis concerns the relationship of metabolic activity in spinal neurons to recovery of motor behavior. Three activity-dependent markers will be examined quantitatively in the acute period and after recovery in the same preparations in which motor behavior is studied: 1) the transneuronal transport method of Jankowska in which WGA-HRP is transported retrogradely from motorneurons to interneurons; 2) cytochrome oxidase (CO) histochemistry; 3) induction of c-fos expression using c-fos protein immunoreactivity. An increase in metabolic activity or transport, or in the number of neurons exhibiting the markers in chronic preparations, compared to acute, would support the hypothesis that metabolic changes contribute to recovery. The fourth hypothesis is that different intraspinal pathways mediate recovery after different lesions. The localization of altered activity may be affected by the specific systems which mediate recovery. This hypothesis will be tested by mapping of WGA-HRP (transneuronal), CO, and c-fos in two different lesion models: hemisection and deafferentation, in which the recovered behavior and the pathways that mediate recovery are considerably different. Differential changes in localization of metabolic activity as a function of lesion type would support the hypothesis.